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House Clinical Pathology > Lipid Metabolism Bullshit > Flashcards

Lipid Metabolism Bullshit Flashcards

1
Q

Lipids are ___phobic compounds but soluble in _______

A

hydro

organic solvents

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2
Q

Major lipids in plasma include fatty acids, triglycerides, cholesterol, phospholipids,__________

A

Terpenes (Vitamins A,E,K)

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3
Q

Increased level of lipids in blood is often associated with ______ diseases which can lead to death

A

cardiovascular

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4
Q

Lipids contained in plasma exist and are transported in the form of _________

A

lipoprotein

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5
Q

Liproproteins are (Covalent or Non-covalent?) assemblies of ____ and ____

A

Non-covalent

lipids and proteins

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6
Q

Structure of liproproteins

Core - _______ and ______

Surface – _____, Proteins and __________ and proteins

A

Triglycerides and Cholesterol esters

Phospholipids

cholesterol esters

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7
Q

Triglycerides are found in ____

A

diet

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8
Q

Triglycerides can not be synthesized in the liver

T/F

A

F

It can

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9
Q

Classification of lipoproteins

Based essentially on _______ determined by ______

A

densities

ultracentrifugation

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10
Q

Classification of liproproteins

Density increases from _______ through lipoproteins of _________, _________ and ___________ , to _________

A

chylomicrons (CM, of lowest density)

very low density (VLDL), intermediate density (IDL)

low density (LDL)

high density lipoproteins (HDL).

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11
Q

The composition of the circulating lipoproteins is static.

T/F

A

F

not static

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12
Q

Circulating liproproteins are in a dynamic state with continuous exchange of components between the various types

T/F

A

T

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13
Q

Lipoprotein(a), or Lp(a), is a normal lipoprotein of known function.

T/F

A

F

atypical
Unknown function

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14
Q

LpA

is (smaller or larger?) and (more or less ?) dense than LDL but has a (different or similar?) composition, except that it contains in addition _________________

A

Larger
More

Similar

one molecule of apo(a) for every molecule of apo B-100.

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15
Q

Apo(a) shows considerable homology with ________.

A

plasminogen

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16
Q

The concentration of Lp(a) in the plasma varies considerably between individuals, ranging from _____ to _______ mg/L.

A

0 to 1000

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17
Q

An elevated concentration of Lp(a) appears to be a/an (dependent or independent?) risk factor for CHD.

A

Independent

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18
Q

• Chylomicrons
• Chylomicrons are formed from ________ (principally ______ and ______ ) in enterocytes

A

dietary fat

triglycerides,
and cholesterol

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19
Q

Chylomicrons

They reach the systemic circulation via the ______

A

thoracic duct

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20
Q

________ are the major transport form of dietary fat.

A

Chylomicrons

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21
Q

Triglycerides constitute about ___% of the lipid in chylomicrons

A

90

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22
Q

Triglycerides are removed from chylomicrons by the action of the enzyme _______, located on the ________ surface of the capillary endothelium of ____ tissue, ____ and _____muscle and ________, with the result that ______ are delivered to these tissues to be used either as _______ or, after re-esterification to triglyceride, for _______.

A

lipoprotein lipase (LPL)

luminal

adipose

skeletal and cardiac ; lactating breast

free fatty acids; energy substrates

energy storage

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23
Q

LPL is activated by _____

A

apo C-II

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24
Q

Apo A and apo B-48 are synthesized in the ____

A

intestine

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25
Q

Apo A and apo B-48 are present in newly formed chylomicrons

T/F

A

T

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26
Q

_____ and _____ are transferred to chylomicrons from HDL.

A

Apo C-II and apo E

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27
Q

As triglycerides are removed from chylomicrons by the action of ____, these become (smaller or larger?)

______,_______,_______,________ are released from the surface of the particles and taken up by ______

A

LPL

Smaller

cholesterol, phospholipids, apo A and apo C-II

HDL.

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28
Q

The chylomicron remnants, depleted of ______ and enriched in ________ are cleared rapidly from the circulation by hepatic?

A

Triglyceride

cholesteryl esters,

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29
Q

Chylomicron major function is the transport of ________

A

dietary triglyceride

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30
Q

chylomicrons also transport dietary cholesterol and fat-soluble vitamins to the liver.

T/F

A

T

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31
Q

Under normal circumstances, chylomicrons cannot be detected in ____ in the ______ state (>___ h after a meal).

A

plasma

fasting

12

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32
Q

Very low density lipoproteins(VLDL)

VLDL are formed from _____ synthesized in the ____ either ____ or by ______ of ______

A

triglycerides; liver

de novo

re-esterification of free fatty acids.

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33
Q

VLDL also contain some ______,_______,______,______

A

cholesterol, apo B, apo C and apo E

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34
Q

VLDL

the apo ___ and some of the apo __ is transferred from circulating ____.

A

E; C

HDL

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35
Q

VLDL

Cholesterol, phospholipids and apo C and apo E are released and transferred to ______.

A

HDL

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36
Q

VLDL

Triglycerides are removed by _______ and is thereby converted into _____.

A

hepatic triglyceride lipase

LDL

37
Q

Triglyceride-rich VLDL are precursors of ___, which comprise mainly ______ and ______

A

LDL

cholesteryl esters and apo B-100.

38
Q

Very low density lipoproteins(VLDL)

•VLDL are the principal transport form of ________ and initially share a similar fate to _______

A

endogenous triglycerides

chylomicrons

39
Q

As the VLDL particles become smaller, phospholipids, free cholesterol and apolipoproteins are released from their surfaces and taken up by ____

A

HDL

40
Q

IDL

More ____ are removed by ______, located on hepatic endothelial cells, and IDL are thereby converted to ____.

A

triglycerides

hepatic triglyceride lipase

LDL

41
Q

Hepatic receptors, also known as ___,____ receptors, are capable of binding _______ and ______ (but not ________).

A

B, E

apo B-100 and apo E

apo B-48

42
Q

Low density lipoproteins (LDL)

• LDLs are the principal carriers of ______, mainly in the form of _____

A

cholesterol

cholesteryl esters.

43
Q

LDL are formed from _____ via _____.

A

VLDL via IDL

44
Q

LDL can pass through the junctions between _________ and attach to LDL receptors on ________ that recognize apo _____.

This is followed by ______ and ———- with release of ________

A

capillary endothelial cells

cell membranes

B-100

internalization and lysosomal degradation

free cholesterol

45
Q

LDL is removed by the _____ and other tissues by a _____- dependent process involving the recognition of ______ by the LDL receptor.

A

liver

receptor

apo B-100

46
Q

LDL receptors are not saturable

T/F

A

F

47
Q

LDL receptors are subject to down-regulation

T/F

A

T

48
Q

Macrophages derived from circulating monocytes can’t take up LDL

T/F

A

F

They can

49
Q

Uptake of LDL by macrophages in the arterial wall is an important event in the pathogenesis of _______.

A

atherosclerosis

50
Q

When macrophages become overloaded with _______, they are converted to ____ cells, the classic components of __________

A

cholesteryl esters

foam

atheromatous plaques.

51
Q

High density lipoproteins(HDL)

HDL are synthesized primarily in the ___ and, to a lesser extent, in ______ cells, as a precursor (‘ _________ ’) comprising phospholipid, cholesterol, ______,——

A

liver

small intestinal

nascent HDL

apo E and apo A.

52
Q

Nascent HDL is ____ shaped

A

disc

53
Q

HDL

In the circulation, it acquires apo ___ and apo __ from ______ and from extrahepatic tissues, and in doing so assumes a _______ conformation.

A

C; A

other lipoproteins

spherical

54
Q

HDL

The free cholesterol is esterified by the enzyme ________________ , which is present in ____ and activated by its cofactor, apo ___. This increases the ____ of the HDL particles, which are thus converted from _____ to ____

A

lecithin-cholesterol acyltransferase (LCAT)

nascent HDL

A-I

density; HDL3 to HDL2.

55
Q

HDL metabolism and reverse cholesterol transport

• Cholesterol in nascent HDL is esterified by _____

A

LCAT

56
Q

Reverse cholesterol transport

Cholesteryl esters are transferred from ___ in exchange for ______, this process being mediated by ____________ protein.

A

HDL

triglycerides

cholesteryl ester transfer

57
Q

Cholesteryl esters are taken up by the liver in _____ and _____.

The triglyceride-enriched HDL2 are converted to HDL3 by ___________ by the enzyme _________, located on the hepatic capillary

A

chylomicron remnants and IDL

the removal of triglycerides

hepatic triglyceride lipase

58
Q

HDL has two important functions

• it is a ____ of _________ for ______

• mediates ___________

A

source; apoproteins for chylomicrons and VLDL

reverse cholesterol transport

59
Q

reverse cholesterol transport is basically taking up of cholesterol from _____ cells and _______ and transferring it to _______, which are taken up by the _____.

A

senescent

other lipoproteins

remnant particles

liver

60
Q

The essential features of lipoprotein metabolism are as follows

• Dietary triglycerides are transported in ______ to ____ where they
can be used as an _____ or ____

• Endogenous triglycerides, synthesized in the _____, are transported in ___ and are also available to _____ as ______ or for __________

A

chylomicrons; tissues; energy source or stored

liver; VLDL; tissues; an energy source or for storage

61
Q

The essential features of lipoprotein metabolism are as follows

• cholesterol synthesized in the ____ is transported to tissues in ___, derived from _____ via ____

• Dietary cholesterol reaches the liver in __________

• HDL acquire cholesterol from _______ and other

A

liver; LDL; VLDL; LDL

chylomicron remnants

peripheral cells

62
Q

Disorders of lipid metabolism

• There are several rare, inherited metabolic diseases associated with the accumulation of lipids in tissues (______________ which can be primary or secondary), and others in which plasma lipoprotein concentrations are reduced

A

Hyperlipidaemias

63
Q

Primary Hyperlipidaemia
Familial hypercholesterolaemia (FH)
Common’ (polygenic) hypercholesterolaemia
Familial dysbetalipoproteinaemia
Familial chylomicronaemia
Familial hypertriglyceridaemia
Familial combined hyperlipidaemia

Familial hyperalphalipoproteinaemia

A
64
Q

Familial hypercholesterolaemia (FH)

This condition is characterized by high plasma ______ concentrations that are present from ———- and do not depend on the _______________

A

cholesterol

early childhood

presence of environmental factors

65
Q

Familial hypercholesterolaemia (FH)

• It is inherited as an autosomal _______ characteristic.

Different mutations can affect _________ synthesis, transport, ligand binding, clustering in coated pits and recycling, but all cause a similar phenotype

A

dominant

LDL receptor

66
Q

Familial hypercholesterolaemia (FH)

• Familial defective_______, in which a mutation in the ______ decreases the ___________, causes a similar phenotype.

A

apo B-100

apo B gene

avidity of LDL for its receptor

67
Q

Familial hypercholesterolaemia (FH)

In all cases, there is a defect in the _____________, and its plasma concentration is increased. In heterozygotes, total cholesterol is typically in the range 7.5–12 mmol/L. The diagnosis is based on the presence of hypercholesterolaemia (>7.5 mmol/L in adults

A

uptake and catabolism of LDL

68
Q

In FH

• There is usually tendon _______ in the individual or close relative, or on DNA evidence of a recognized mutation.

A

xanthomata

69
Q

‘Possible’ FH is considered to be present in patients who do not meet these definitive criteria, but who _________________________ together with ___________________

A

have the same degree of hypercholesterolaemia

a family history of premature CHD or hypercholesterolaemia.

70
Q

Common’ (polygenic) hypercholesterolaemia

• The distribution of plasma cholesterol concentrations in relatives is _____
• More frequently, when the family of an individual with hypercholesterolaemia is studied, a ___________ is found, consistent with the ________ being influenced by _______.

This entity has been termed ‘ _______ ’ or ‘_____’ hypercholesterolaemia

A

bimodal

continuous distribution

plasma cholesterol; several genes

common; polygenic

71
Q

Difference between familial hypercholesterolemia and Common’ (polygenic) hypercholesterolaemia

A

Plasma cholesterol in common is not generally as high as in FH

Common is more influenced by environmental factors

72
Q

Common’ (polygenic) hypercholesterolaemia

The significance of this condition again lies in its relationship to the risk of _________, and the principles of management are (similar or different ?) to those for FH.

A

coronary artery disease

Similar

73
Q

common (polygenic) hypercholesterolaemia

In polygenic hypercholesterolaemia, however, _________ alone may sometimes be adequate to lower the cholesterol concentration to acceptable levels.

A

dietary treatment

74
Q

Familial dysbetalipoproteinaemia

• This condition is characterized clinically by the presence of ______ in the _________ and by ________

the latter tend to occur over ________ and, unlike tendon xanthomata, are _____ in colour.

A

Fat deposits ; palmar creases

tuberous xanthomata

bony prominences ; reddish

75
Q

Familial dysbetalipoproteinaemia

• In some patients, ______ xanthomata are present
• Biochemically, the condition is characterized by the presence of an excess of ______ and ______

_______ are sometimes also present.

A

eruptive

IDL and chylomicron remnants

chylomicrons

76
Q

Familial dysbetalipoproteinaemia

Total cholesterol and triglyceride concentrations are ______, typically to ________ values.

A

elevated

approximately equal

77
Q

Familial dysbetalipoproteinaemia

Patients have increased risk of _______________________ disease

A

both coronary and peripheral Cardiovascular

78
Q

Familial chylomicronaemia

• Fasting chylomicronaemia is a feature of two rare hyperlipidaemias, both having an autosomal ______
• deficiency of the enzyme _____
• deficiency of ______, which is required for activation of this enzyme
• The result in each case is a failure of _________ from the bloodstream.

A

recessive

lipoprotein lipase

apo C-II

chylomicron clearance

79
Q

Familial chylomicronaemia

• Presentation is usually in _____, with _____ xanthomata, recurrent abdominal pain due to _______ and sometimes ______.

A

childhood

eruptive

pancreatitis

hepatosplenomegaly

80
Q

In Familial chylomicronaemia Lipaemia retinalis may also be present.

T/F

A

T

81
Q

Familial chylomicronaemia

• Management involves giving a _______, with substitution of some fat by ______

A

low fat diet

triglycerides

82
Q

Familial hypertriglyceridaemia

• This condition is usually associated with an excess of ______ in plasma.

It is usually not manifest until ______.

A

VLDL

adulthood

83
Q

Familial hypertriglyceridaemia

The molecular basis is uncertain; there is increased hepatic synthesis of ______.

Inheritance is autosomal ______.

A

VLDL

dominant

84
Q

Familial hypertriglyceridaemia

Triglyceride concentrations are not usually higher than ___ mmol/L,

A

5

85
Q

Familial combined hyperlipidaemia

• This is due to hepatic overproduction of _____, leading to increased ____ secretion and increased production of __________.

Either _______ or _______ , or both, may be elevated

A

apo B; VLDL

LDL from VLDL

plasma cholesterol or triglyceride

86
Q

Familial combined hyperlipidaemia

• Hyperlipidaemia with increased risk of coronary artery disease is usually present
T/F

A

T

87
Q

Familial hyperalphalipoproteinaemia

• Hypercholesterolaemia is due to an increase in only the _____ fraction, which may be present in other members of the family
• CHD risk may be ___eased, and _________ treatment is required

A

HDL

decr

no specific

88
Q

Familial hyperalphalipoproteinaemia

The existence of this condition underlines the need to measure _________ in patients with hypercholesterolaemia.

Generally, if total cholesterol is greater than 7 mmol/L, there will always be an increase in _____, but, even then, measurement of _____ helps in the assessment of CHD risk

A

HDL cholesterol

LDL

HDL

89
Q

The management of lipid disorders

Essentials of management is based on
• Adequate ______
•______ modification
• Use of drugs like _______,_______,________
• Proper management of _________ that increaser risk of CVD eg, ____

A

risk assessment

Lifestyle

statins, HMG co A reductase inhibitor, fibrates

Secondary conditions; DM

House Clinical Pathology (45 decks)

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